The concentration of Na inside vascular smooth muscle cells is an important regulator of vascular smooth muscle function. Although Na efflux from these cells via the Na, K pump has received much attention, little is known about the sarcolemmal translocation pathways which mediate Na influx. Prior studies have shown that Na flux into arterial strips is increased in several forms of experimental hypertension, but the translocation pathways involved are not known. These studies will test the hypothesis that specific transport mechanisms which mediate Na influx are present in the sarcolemma of vascular smooth muscle cells, and that an increase in the activity of one or more of these transport systems is found in mineralocorticoid induced hypertension. It is proposed to test for the presence of, and characterize five specific Na translocation pathways in sarcolemmal vesicles from canine superior mesenteric artery: 1) Na diffusion; 2) Na channels; 3) Na/H exchange; 4) Na/K/Cl cotransport; 5) Na/Ca exchange. In addition, the effects of aldosterone in-vitro, and DOCA-salt hypertension on the activities of these pathways will be determined. These studies will contribute to the fundamental understanding of Na metabolism in vascular smooth muscle cells, under normal and abnormal conditions. Such information may help establish the pathogenesis of certain hypertensive states, and lead to the development of specific therapies for these diseases.